This work is designed to investigate the neurological mechanisms involved in the return of function following regeneration of lesioned peripheral nerves in mammals. It has already been shown in this laboratory that regeneration of cutaneous sensory fibers involves the apparent return of the specific receptor properties which a given fiber had before being lesioned. It has also been shown that at least one class of receptors, the Type I cutaneous mechanoreceptors, tend to reappear at those loci where such receptors were found before nerve injury. Moreover, the return of these receptors was more complete, and showed a higher degree of coincidence, after nerve crush then after transection. By extending the neurophysiological methods used in these studies, including recording from individual sensory neurons, the question of why regeneration is better after nerve crush than after nerve transecton will be pursued. As part of this work, the mechanism by which Type I neurons are guided back to appropriate terminal locations will be determined. Other factors which will be considered include the effects of denervation time, the extent to which transection neuromas act as a barrier to regrowing fibers, and the influence of the extraneural environment on regeneratig sprouts.